Autonomic dysreflexia

Abstract

Autonomic dysreflexia (AD) may complicate spinal cord injured (SCI) subjects with a lesion level above the sixth thoracic level. There are several ways to remove triggering factors and, furthermore, new trigger mechanisms may be added by the introduction of new treatments. New data about the pathogenic mechanisms have been suggested in recent years as well as signs of metabolic effects associated with the reaction. This review of the syndrome includes clinical aspects of the AD reaction; the known pathogenic mechanisms, the incidence and prevalence and triggering factors. AD is associated with some cases of severe morbidity, including cerebral haemorrhage, seizures and pulmonary oedema. Symptomatic as well as specific treatments are discussed. Finally, some further questions are raised by the necessity of a proper definition of the syndrome, the revealing of the underlying pathophysiology, and new investigations concerning incidence and prevalence.

Selective activation of muscle and skin nociceptors does not trigger exaggerated sympathetic responses in spinal-injured subjects

“…1 However, a common definition found in the literature for the cause of AD resembles the following: 'yany stimulus that might cause pain in a person without spinal cord injury is capable of triggering AD.'. 6,7 Our study has demonstrated that in a population of spinal cord-injured subjects who are capable of becoming dysreflexic, stimuli that cause strong pain in able-bodied subjects did not trigger autonomic dysreflexia.…”

“…It is believed that the increase in blood pressure is initiated and maintained by a sympathetically mediated vasoconstriction in muscle, skin and splanchnic vascular beds. 1 The increase in blood pressure can have dangerous consequences, including stroke and death. AD is triggered by stimuli originating below the level of lesion.…”

Early autonomic dysreflexia

“…Autonomic dysre¯exia is considered to occur when, in response to an appropriate stimulus, there is an increase in systolic blood pressure by at least 20% combined with at least one of the following symptoms: sweating, chills, cutis anserine, headache or¯ushing. 9 Abnormal sweating is regarded as an outstanding component in symptomatology and, in the absence of blood pressure records as Figure 1 Case 1 sustained a complete transverse spinal cord lesion below the sixth cervical segment on 2 May. He was being treated by intermittent catheterisation.…”

“…Stimuli originate below the level of the lesion from the skin, abdominal or pelvic viscera, skeletal muscles or, most commonly, distension of the bladder. The accepted criterion of autonomic dysre¯exia is an increase in systolic blood pressure by at least 20%, 9 sometimes combined with bradycardia and occasional cardiac dysrhythmias. This may be accompanied by one or more of the following symptoms: sweating in areas above and around the lesion depending on the level of the lesion, muscle spasm, paraesthesiae in the neck and shoulders, headache, a feeling of fullness in the head, pallor followed by¯ushing of the face.…”

“…Elevation of blood pressure and symptoms decline after removal of the stimulus. 9 Case histories Patient 1 (1971 original case, Table 1) sustained a complete transverse spinal cord lesion below C6 on 2.5.70 as the result of a motor cycle accident. Seven days after injury, tendon re¯exes were absent, but anal re¯ex was present.…”